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N&PD Moderators: Skorpio
What it takes to recover from being on a benzo like clonazepam =time off the drug (?)
- Thread starter Kdem
- Start date
i am not 100% of what youre asking, but im assuming you mean, what does it take to come off of a benzo? depending on your habit, it COULD take up to several months (6 months for severe addiction), and a lot of mental fighting. Tapering is usually the best way to go, just make sure you make it a slow taper. Never stop cold turkey, or you could have seizures.The exercise and sun exposure (leading a full life yes but thats vague), speed up the recovery process and contribute to health in general.
It's not like you can't recover without them but it will be slower and less 'complete'.
Why do you ask?
No offense and it is not my business but yeah if you ask here then I gotta ask in return: how does this matter in the decision to get off clonazepam? I've followed your threads on it for quite some time and don't get me wrong (yes I'm usually direct / harsh): I do sympathize and yes I do understand the challenges and hurdles as I have withdrawn from benzos myself.
The real answer to what it takes, is the firm realization and decision that you must go for it and just pull through however you can simply because staying on it indefinitely is so much worse. I get that it's frightful because of what may surface and about losing control, but what you can do is take measures to prepare for mental or physical issues and just confront it even if it's an ugly prospect. In my experience with being inactivated and on benzos or ketamine or other things, is that in my case at least, the strength to act is eroded, eaten away. Sooner or later in my case something triggered me to come into action anyway, and then when I did to just pull through.
So, from my perspective, yes reupping your possibility to go outside, exercise (will be painful but just do it for your health), all of that will help, but don't let any of it stall you as a distraction. For me, the trigger to just get the ball rolling has usually been among the most elusive things, so I can't really offer you a real solution... but staying right where you are isn't helping (I'm confident considering what you told us and that you keep posting). The benzos also pull such a haze over your eyes keeping you dulled... for me the best thing usually was to gather some critical mass, some momentum leading me to realizations and a moment of clarity so that I could at least initiate something.
Just like CBT separates the rational from the irrational, so you must make the same separation and prepare for what you can and forget about the endless irrational stuff and just start the best line of treatment you can arrange. You mostly need to be harsh to yourself right now and wake up so that you can get things going. Endless preparation and theorizing does not substitute for action.
Fuck, yes it's very hard. It's ridiculous to really act compared to the other stuff, but that's the only real thing cause the rest doesn't matter if you never do.
take care
keep it up and go for it
Ligaturd
Bluelighter
Some people who have been on it for an extended period of time find that it takes years to recover. It would depend on the dosage, how long you have been using and whether or not you go off of it cold turkey (cold turkey can cause excess excitotoxicity and therefore more damage). It is worth it though, in the end. Good luck.@Solipsis,
I best not venture into the details ...
But it is different if you've been on 2 mg clonazepam a day, every single day for many years rather than 'on benzos' for a few months, possibly alternating benzos.
The stuff is at least partly paradoxical ...
And it is not as if I didn't have only partly related issues like general exhaustion, preexisting insomnia and some others as well. Having a GP that doesn't take me seriously with a 'it's just a pill' attitude.
If I had not been on that lorazepam for almost three months I wouldn't be in this mess. That was 2 mg BID=4 mg a day. GP's idea, my mistake to accept that 'taper'.
Lorazepam is (or rather, was) somewhat hypnotic, sedating, amnestic. Much more so than clonazepam. When I developed tolerance and dependence things went to hell ...
I'm sure that lorazepam has a relatively high affinity for the alpha1 and alpha5 subunit. Aside from other receptors/brain areas. When I read that diazepam also has a relatively high affinity to the alpha1 and 5 receptors compared to clonazepam (I tried diazepam!) I was reluctant to force the issue ... And diazepam is so short acting and different.
I am still in lorazepam withdrawal ... that stuff is so nasty. I let the GP make a mistake (I had other preferences) and I have to deal with the consequences.
In a nutshell, if I had not taken lorazepam, if my health was not a mess I wouldn't have had these problems with the clonazepam !
Real exercise after clonazepam is bad ... it may feel fine, but there are consequences later (insomnia and other serious issues). Anyway, I don't have the 'genes' for that kind of thing. It has been a hell of a fight. I've been pondering phenazepam, but importing that stuff as a RC while knowing very little about it and becoming dependent on it ...
Yeah, anybody got any ideas about getting off a paradoxical benzo after long term use ? I realize that it is at least partly paradoxical, now it's worse and my health is worse ... The literature only discusses this for short term use.If anyone likes some reading, I have been trying to find information about benzo specific binding to receptors. Very hard to find anything.
This one compares alprazolam and lorazepam, I just copied this from a PDF (can't post attechments), read or do not read.
Br. J. Pharmacol. (1990), 101, 839-842
Differential effects of chronic lorazepam and alprazolam on
benzodiazepine binding and GABAA-receptor function
Wendy R. Galpern, 'Lawrence G. Miller, David J. Greenblatt & Richard I. Shader
Division of Clinical Pharmacology, Departments of Psychiatry and Pharmacology, Tufts University School of Medicine and New
England Medical Center, Boston, MA, U.S.A.
1 Chronic benzodiazepine administration has been associated with tolerance and with downregulation
of y-aminobutyric acidA (GABAA)-receptor binding and function. However, effects of individual benzodiazepines
on brain regions have varied.
2 To compare the effects of chronic lorazepam and alprazolam, we have administered these drugs to
mice for 1 and 7 days (2 mg kg'- day 1) and determined benzodiazepine receptor binding in vivo with and
without administration of CL 218,872, 25 mgkg' i.p., and GABA-dependent chloride uptake in 3 brain
regions at these time points.
3 Benzodiazepine binding was decreased in the cortex and hippocampus at day 7 compared to day 1 of
lorazepam, with an increase in CL 218,872-resistant (Type 2) sites in both regions. Maximal GABAdependent
chloride uptake was also decreased in the cortex and hippocampus at day 7.
4 Binding was decreased only in the cortex after 7 days of alprazolam, with no significant change in
Type 2 binding. Maximal GABA-dependent chloride uptake was also decreased only in the cortex.
5 These data suggest that the effects of chronic benzodiazepine administration on the GABAA-receptor
may be both region-specific and receptor subtype-specific.
Introduction
In clinical use, chronic benzodiazepine administration is
associated with the development of tolerance to anticonvulsant
and hypnotic effects (e.g., Greenblatt & Shader,
1978). Tolerance has also been observed in a number of
animal models with a variety of benzodiazepines, including
'classical' benzodiazepines and the newer triazolobenzodiazepines
(Garratt et al., 1989). In previous
studies, we demonstrated the development of tolerance during
chronic administration of the classical benzodiazepine lorazepam
(Miller et al., 1988a) and the triazolobenzodiazepine
alprazolam (Miller et al., 1989c). In both cases, tolerance was
associated temporally with benzodiazepine receptor downregulation
and decreased GABAA-receptor function. Similar
results have been obtained by other investigators for flurazepam
(Tietz et al., 1986) and diazepam (Marley & Gallager,
1989).
However, our results indicated that receptor downregulation
produced by alprazolam and lorazepam had differing
regional specificity. Receptor alterations induced by
lorazepam occurred in the cortex, hypothalamus, and hippocampus,
whereas those associated with alprazolam occurred
in the cortex and hypothalamus only. A possible mechanism
for this discrepancy is differential effects of the two drugs on
benzodiazepine receptor subtypes (Sieghart, 1989), although
binding studies do not indicate a substantial difference in this
regard (Haefely et al., 1985). We did not assess regional specificity
for y-aminobutyric acid (GABA)-dependent chloride
uptake, although other investigators have demonstrated
effects in the cortex but not the cerebellum after chronic diazepam
(Marley & Gallager, 1989).
To assess possible region-specific effects of lorazepam and
alprazolam during chronic administration, we evaluated benzodiazepine
binding in vivo and GABA-dependent chloride
uptake in several brain regions both before (day 1) and after
(day 7) the development of tolerance to both compounds. In
addition, we evaluated the relative proportion of benzodiaze-
1 Author for correspondence at Box 1007, New England Medical
Center, 750 Washington St., Boston, MA 021 11, U.S.A.
pine subtype binding by use of the subtype-specific ligand CL
218,872 (Sato & Neale, 1989).
Methods
Male CDt mice, 6-8 weeks of age, were obtained from
Charles River Laboratories (Wilmington, MA), given food and
water ad libitum, and maintained on a 12 h light/dark cycle.
Lorazepam and alprazolam (2mgkg- day-') were dissolved
in PEG 400 and administered by subcutaneously
implanted osmotic pumps as previously described (Miller et
al., 1988a). Day 1 was chosen as a point before the development
of tolerance and receptor alterations, and day 7 as a
point associated with tolerance and receptor changes (Miller
et al., 1988a). Benzodiazepine receptor subtypes were distinguished
by use of CL 218,872, which appears to bind preferentially
to Type 1 sites (Sieghart, 1989). CL 218,872 was
dissolved in ethanol and diluted with saline to a final ethanol
concentration of 0.1%. Vehicle contained 0.1% ethanol
diluted with saline.
Benzodiazepine binding in vivo was performed as previously
described (Miller et al., 1988a). Briefly, mice were injected i.v.
with 3PCi [3H]-Rol5-1788. After 20min, animals were killed
and brains rapidly removed and dissected on ice. After the
brain regions had been weighed they were dissolved in Protosol
(400C for 24 h) and then counted by scintillation spectrometry.
For subtype specific binding mice were injected with CL
218,872, 25 mgkg1- i.p., 30 min before the radioligand.
GABA-dependent chloride uptake was performed as previously
described (Miller et al., 1988a). Briefly, cortical synaptoneurosomes
were prepared and resuspended in assay
buffer (145 mm NaCI, 5 mM KCI, 1 mM MgCl2, 1 mM CaCl2,
10mM HEPES, pH 7.4). After incubation for 10min at 300C,
lOO1ul of membrane suspension mixed with 100,pl of a solution
containing muscimol (1-50pM) and 36C-, 0.2 pCimP'1
assay buffer. After 6s the incubation was terminated by addition
of 0.5 ml cold assay buffer containing 6pM picrotoxin and
filtration on Whatman GF/C filters by a Brandel M24 apparatus.
Filters were washed twice with cold buffer and counted
by scintillation spectrometry.
,'-. Macmillan Press Ltd, 1990
840 W.R. GALPERN et al.
[3H]-Rol5-1788 (flumazenil, spec. act. 80Cimmol-') and
36Cl- (spec. act. 25 Ci mg- 1) were obtained from New
England Nuclear (Boston, MA). Muscimol was obtained from
Sigma and polyethylene glycol 400 (PEG 400) from J.T. Baker
(St. Louis, MO). Osmotic pumps were obtained from Alza
(Palo Alto, CA). Alprazolam was a gift from Upjohn
(Kalamazoo, MI), lorazepam from Wyeth (Philadelphia, PA)
and CL 218,872 from Dr Joseph Moerschbaecher.
Data were analysed by Student's t test, the Mann-Whitney
test, or analysis of variance with Dunnett's test.
Results
Benzodiazepine receptor binding in vivo was significantly
decreased in cortex and hippocampus at day 7 compared to
day 1 of lorazepam (cortex, day 1: 1609 + 191 fmol g-1; day
7: 1182 + 150fmolg-1; n = 6-9; P < 0.05; hippocampus, day
1: 2509+254fmolg-1; day 7: 1718 + 14Sfmolg';
mean + s.e., n = 6-9, P < 0.05; Figure 1). These results are
similar to those previously obtained (Miller et al., 1988a),
except that decreased binding in the hypothalamus did not
reach significance (P < 0.10). Differences in the cerebellum
were not significant (day 1: 668 ± 18fmolg-', day 7:
277 + 27fmolg-; n = 6-9; P > 0.15). In contrast, Type 2
benzodiazepine receptor binding (binding remaining after
administration of 25mgkg-t CL 218,872) was increased in
the cortex and hippocampus at day 7 compared to day 1.
Type 2 binding was increased both in absolute terms (cortex,
day 1: 254 + 14fmolg '; day 7, 405 + 45fmolg-'; P < 0.05;
hippocampus, day 1: 554 + 23 fmol g- 1; day 7:
754 + 91 fmol g'- ; P < 0.05) and even more dramatically as a
percentage of total specific binding (Figure 1 inset). Changes
in Type 2 binding in the cerebellum (day 1: 241 + 18 fmol g1;
day 7: 277 + 27fmolg-'; P > 0.15) and other regions were
not significant.
For alprazolam, benzodiazepine receptor binding in vivo
was significantly decreased in the cortex at day 7 compared to
day 1 (day 1: 1918 + 127fmolg'-; day 7:
1595 + 127fmolg1; n = 7-9; P < 0.05; Figure 2). No alterations
in other brain regions were observed (hippocampus,
day 1: 2522 + 214fmolg-1; day 7: 2436 + 145fmolg-;
n= 7-9; P>0.40; cerebellum, day 1: 914 + 82fmolg1; day
40-
3000
2000~~ ~~~~~0
0)~~ ~ ~~~~~2
7E5 2000 -Sj 1
CL
0
HI HY CX CB P-M
Brain region
Figure 1 Effects of chronic lorazepam on benzodiazepine binding in
vivo. Binding was determined by specific uptake of [3H]-Rol5-1788.
Results are mean and vertical bars show s.e.mean, n = 7-10.
CB = cerebellum, CX = cortex, HI = hippocampus, HY = hypothalamus,
and P-M = pons-medulla. *P < 0.05 vs. day 1. Inset: effects of
chronic lorazepam on Type 2 benzodiazepine binding. Binding was
determined as above after administration of CL 218,872, 25 mgkg'-
i.p. Results are means expressed as a percentage of total binding,
n = 6-9. Results in cortex and hippocampus for lorazepam are significant
(P < 0.05). (0) Day 1; (0) day 7.
0)~~~~~~~~2
E 2000-
0)~~~~~~~~~ C~~ ~ ~ ~ ~ ~~C
1C3D_
0
HI HY CX CB P-M
Brain region
Figure 2 Effects of chronic alprazolam on benzodiazepine binding in
vivo. Binding was determined by specific uptake of [3H]-Rol5-1788.
Results are mean and vertical bars show s.e.mean, n = 7-10.
CB = cerebellum, CX = cortex, HI = hippocampus, HY = hypothalamus,
and P-M = pons-medulla. *P <0.05 vs. day 1. Inset: effects of
chronic alprazolam on Type 2 benzodiazepine binding. Binding was
determined as above after administration of CL 218,872, 25 mgkg'-
i.p. Results are means expressed as a percentage of total binding,
n = 6-9. Results in the cortex are not significant. (0) Day 1; (0) day
7.
7: 818 + 77fmolgt; n = 7-9, P > 0.30). Unlike in previous
studies (Miller et al., 1989c), alterations in the hypothalamus
did not achieve significance (day 1: 2141 + 214 fmol g-1; day
7: 1809 + 214fmolg-1; n=7-9; P < 0.15). Type 2 benzodiazepine
receptor binding was slightly but not significantly
increased in the cortex at day 7 compared to day 1, either as
specific binding (day 1, 295 + 20 fmol g-'; day 7,
332 + 25 fmol g-1; P < 0.15) or as a percentage of total specific
binding (Figure 2 inset). Changes in Type 2 binding in the
hippocampus (day 1: 527 + 36fmolg-'; day 7:
618 + 41 fmol g-1; P > 0.10), cerebellum (day 1:
223+14fmolg-1; day 7: 241 + 18fmolg-1; P>0.20) and
other brain regions were not significant.
GABA-dependent chloride uptake in the cortex was
decreased at day 7 compared to day 1, as previously found
(Miller et al., 1988a; Figure 3). Maximal chloride uptake was
decreased, but the EC50 for muscimol was not altered (day 1:
3.2 pm; day 7; 3.8 pM). A similar decrement in maximal uptake
without a change in the EC50 was observed in the hippocampus
(EC50: day 1, 4.2 uM; day 7, 3.4 gM), but no changes in
either maximal uptake or EC50 for muscimol were observed in
the cerebellum.
For alprazolam, maximal GABA-dependent chloride
uptake was decreased at day 7 compared to day 1 (Figure 4)
with no change in the EC50 (day 1: 3.9 pm; day 7: 3.1 pM), as
previously demonstrated (Miller et al., 1989c). A small, non
significant decrease in uptake was observed in the hippocampus,
and no changes in the EC50 for the maximal uptake
of muscimol were observed in the cerebellum.
Discussion
These data corroborate previous studies indicating downregulation
of GABAA-receptor binding and function after
chronic lorazepam and alprazolam administration (Miller et
al., 1988a; 1989c). For both lorazepam and alprazolam,
decreases in benzodiazepine binding and chloride uptake were
observed in the cortex at day 7 compared to day 1. Binding
was decreased in the hippocampus after lorazepam but not
alprazolam, as previously found. For both drugs decreases in
binding in the hypothalamus did not achieve significance, in
contrast to previous findings (Miller et al., 1988a; 1989c).
The present study extends our previous data in two
respects. First regional alterations observed in
DIFFERENTIAL EFFECTS OF LORAZEPAM AND ALPRAZOLAM 841
a20 b c
20 0 453~0~~~~~0 10 0
.5 10~~~~~~~~~~~~~~0
E o 0 0
CE 0 1020 3040 50 010b'2030O 4050 0 1020 3040 50
Muscimol (>M)
Figure 3 Effects of chronic lorazepam on GABAA-receptor function in (a) cortex, (b) hippocampus and (c) cerebellum. Chloride
uptake was determined in the presence (1-50pM) and absence of muscimol. Maximal uptake was decreased at day 7 (a) compared to
day 1 (0) for lorazepam in the cortex and hippocampus (P < 0.05). Results are means of 3-5 determinations at each point.
Z 20a 50. 20C
4- 0 400 15 0
.1C 1000 200 10 0
CLI 10 lo10-
E o 0 0O
C 0 10 2030 40 50 0 10 20 30 40 50 0 10 20 30 40 50
Muscimol (AM)
Figure 4 Effects of chronic alprazolam on GABAA-receptor function in (a) cortex, (b) hippocampus and (c) cerebellum. Chloride
uptake was determined in the presence (1-50pM) and absence of muscimol. Maximal uptake was decreased at day 7 (@) compared to
day 1 (0) for alprazolam in the cortex (P < 0.05). Results are means of 3-5 determinations at each point.
GABAA-receptor function were analogous to those previously
observed in binding studies. That is, lorazepam effects on
chloride uptake were observed in cortex and hippocampus but
not cerebellum, and alprazolam in cortex alone. Alterations in
cortex but not cerebellum are similar to results obtained for
diazepam by other investigators (Marley & Gallager, 1989). In
addition, the association of changes in benzodiazepine binding
and GABA-dependent chloride uptake observed in this study
has been observed in most (Lopez et al., 1990a,b; Miller et al.,
1989a,b), but not all (Lopez et al., 1989), previous studies.
Second, alterations in binding after chronic lorazepam
appear to have a greater effect on Type 2 benzodiazepine
receptors compared to Type 1 sites. Not only did the binding
in the cortex and hippocampus resistant to CL 218,872 (Type
2) increase after 7 days of lorazepam, but the percentage of
Type 2 sites increased substantially. A non-significant increase
in Type 2 binding was observed with alprazolam. These data
suggest that chronic benzodiazepine treatment may preferentially
affect one subclass of benzodiazepine receptors,
despite the use of a ligand (lorazepam) which does not appear
to bind differentially at the two sites. An alternative explanation,
although it remains speculative, is that chronic lorazepam
administration leads to altered receptor structure so that
the ligand used, Rol5-1788, bound preferentially to one site.
For both binding and functional studies, results of chronic
(7 days) treatment were compared to short-term treatment (1
day) as in previous studies. Short-term treatment rather than
vehicle is the appropriate comparison for chronic treatment,
since the presence of a benzodiazepine in the tissue would be
expected to alter the results of both binding and functional
assays. We have previously demonstrated that brain concentrations
achieved by implanted pumps are unchanged at days
1 and 7 for both lorazepam and alprazolam (Miller et al.,
1988a; 1989c), indicating that the comparison of these time
points is appropriate.
Substantial neurochemical evidence (e.g., Sato & Neale,
1989; Sieghart, 1989), and recently molecular biological evidence
(e.g., Shivers et al., 1989; Olsen & Tobin, 1990), support
the existence of multiple benzodiazepine receptors. A number
of benzodiazepine, fl-carboline, and non-benzodiazepine
ligands have been demonstrated to distinguish between receptor
subtypes. The identification of multiple variants of the a, fl
and y subunit mRNAs, together with in situ hybridization
studies demonstrating region-specific localization of several
subunits (Shivers et al., 1989), strongly support the existence of
receptor subtypes with different structural and perhaps functional
characteristics. Recent transfection studies confirm differences
in benzodiazepine binding related to the a, versus a3
subunits (Pritchett et al., 1989). Thus, it is likely that several
GABAA-receptors exist with differing benzodiazepine binding
characteristics and these subtypes are likely to have differing
regional specificity.
Several mechanisms might account for the alteration in the
percentage of Type 1 and Type 2 sites in cortex associated
with chronic lorazepam. It is possible that lorazepam might
mediate interconversion of the two receptor states, either at
the genome or post-translationally. Alternatively, the lack of
alteration in subtype binding in cerebellum, where Type 1
sites predominate, may indicate a specific effect of chronic
lorazepam on Type 2 sites. Finally, chronic lorazepam might
alter receptors such that the radioligand used, Rol5-1788,
binds preferentially to one site.
Our results suggest region-specific effects for chronic lorazepam
and alprazolam on binding and function at the
GABAA-receptor. It is unlikely that these effects are related to
dose or drug concentration, since the same doses were used
and the regimen used maintains similar chronic drug concentrations
in brain. However, it remains possible that different
concentrations of individual benzodiazepines are required to
alter receptors in different regions. Our results over a broad
dose range for lorazepam (1-lOmgkg- day-') argue against
this hypothesis (Miller et al., 1988b). That is, results are
similar with different lorazepam doses but are distinct from
alprazolam at each dose evaluated. Rather, it appears more
likely that chronic lorazepam downregulates benzodiazepine
sites in the cortex and hippocampus, with a preference for
Type 2 sites. In contrast, alprazolam downregulates receptors
in the cortex only, without a significant effect on either receptor
subtype. Effects on GABAA-receptor function exhibit
similar regional specificity. It is possible that these differential
effects are due to the binding characteristics of lorazepam and
alprazolam. It is also possible that either compound might
effect another neurotransmitter system, with indirect effects on
the GABAA complex. Finally, the two drugs might differentially
affect the GABAA-receptor subunit gene expression. Additional
studies examining the effects of these compounds on the
GABAA-receptor gene regulation may shed light on this
hypothesis.
The authors thank Jack Heller and Young Shim for technical assistance.
Supported in part by grants DA-05258, MH-34223, and AG-
00106 from the U.S. Public Health service. L.G.M. is the recipient of a
Faculty Development Award in Clinical Pharmacology from the
Pharmaceutical Manufacturers Association Foundation.
842 W.R. GALPERN et al.
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TIETZ, E.I., ROSENBERG, H.C. & CHIU, T.H. (1986). Autoradiographic
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Exp. Ther., 236, 284-291.
(Received April 17,1990
Revised July 4, 1990
Accepted July 12, 1990)
adder
Bluelighter
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I think Solipsis gave you some good advice. I don't know how long he was on benzodiazepines and at what doses, but if you're looking for a long-term benzodiazepine dependent person who managed to quit this shit for good, then here I am. I took benzodiazepines for around 9 years with the last 6 years of that being at least 6mg of clonazepam a day which I had regularly prescribed by a psychiatrist who obviously didn't care much about me and my future or basically my life. I was 14 when I started taking benzodiazepines and very soon I found myself taking them every day at excessive doses especially lorazepam (7.5mg was a usual dose for me throughout a day) and estazolam.
Anyway, what you should understand is that to quit now it doesn't matter how you found yourself trapped in clonazepam dependence in the first place. Blaming yourself or other people will not help at all but only further distract you from your goal of quitting. Obviously if you started taking benzodiazepines due to psychological/emotional problems that you couldn't have resolved otherwise, you can be sure that they are still there and most likely they have built up over the years, and you will sooner or later face those problems after quitting, the deepest problems may not hit you during the first phase of the withdrawal which is rather general anxiety that doesn't need additional fuel, but they will come out, that's what you eventually want though. I'm still wrapping my head around the sources of my problems 3 years after quitting benzodiazepines, often it feels like learning the very basics about social interactions, but that's how it is with benzodiazepines, they deprive you of so much emotions and feelings that you exist on a completely different level than people whose emotions are not restrained at all. For example I notice healthy people cry in certain situations while I still can't, partly due to buprenorphine, I choke on my own pain and am unable to let it out. I mean that it is a long and painful process, but it has generally felt extremely good for me to start feeling things I forgot existed while on benzodiazepines right from the beginning of my withdrawal despite the anxiety and pain. Still, at times anxiety hits me harder now than ever before and I feel as if I were to explode or die of a heart attack, I know learning to deal with this on my own is necessary though. Feeling is necessary, emotions and feelings are what motivates or unmotivates you, benzodiazepines shut them off all, and deep down inside you know it yourself, that's why you want to quit. That's why I decided to quit opioids and benzodiazepines, I wanted to start feeling emotions to the fullest again, I wanted to be able to be the true myself to other people, I wanted to be able to do things that I used to love and that need focus and working memory which I lacked on drugs.
Your problem now is not finding the right benzodiazepine to switch to or in learning more details about how benzodiazepines affect your brain, it is to make a conscious decision and follow it knowing the consequences. It is a path that many people took and managed to quit, so why not you? Granted each case was unique as everyone deals with stuff in their own way.It's harsh for us to give advice like that and I appreciate that you have further health complications and understand that it is one hell of a fight for you. And also that it may be heavier than what I had to go through.
The point is not that we think you should just do it effortlessly or without dangers or that it's easy, but that it's good to gather what energy you can muster and invest it in the things that matter instead of wasting energy on things that are unlikely to play a role in the success of your withdrawal.
When there are health complications like you have, focus with your physician on managing it, similar to CBT you could separate what is rational and irrational or what *can* be prepared for and dealt with and what has limited solutions - you might just have to learn to accept that. Trust that a key factor in your quitting may be your mentality and perseverence, while also understanding that benzo may very well have eroded things like your willpower.
Nevertheless, what's left of that willpower and how you use it is important; And your resolve to choose to pull through whatever happens and to be determined that distractions and concerns you have about not being able to manage or survive mentally or physically can be like self-fulfilling prophecies.
No, it's difficult to say how you will be affected and what you will be left with, but as long as you fret about the unpredictability you can be certain that inaction leaves you right where you are. So the question becomes whether it's a way to live or whether it is better to get treated and heal, even if it's hazardous, full of complications and hardship.
I may not have the same health problems or sensitivities (although in my case there is psychiatric comorbidity so yeah each case is unique like adder said), but I do have experience with trying to learn about every minute detail about something and postponing acting on any of it, getting nowhere and having wasted time.
I'm sorry.Well, I just don't have a doc I can rely on. In fact, the current GP has been a disaster. The local medical system is a mess. And the drug is at least partly paradoxical.
You could say that the dependence and my health issues are 'mixed', in the sense that my health also affects my brain and my hormones. For example, imagine the effects of long term insomnia and physical stress on the brain. In a situation like this, you can't just take an antidepressant for stress, sleep or mood. You can't take a hypnotic (I can't) for sleep. There were problems I couldn't get treatment for (e.g. 'get off the drug first')
And I'm not saying medically nothing is possible. I just think that what might help is way beyond what is common and accepted as medical practice.
I think that my issues are to a great extent neurological and hormonal. Plus a few other things I won't mention here.
I wonder if it's not gonna end up like CT (which would be extreme, as in duration and intensity), tapering off with a different benzo is hard at best. Diazepam is SO different and IMO not suitable, no to mention waking up after 2-3 hours when the drug wears off. I've been pushed beyond my limits by in total 4 docs.
Earlier this year I tried to get gabapentin or Lyrica prescribed. I just should have bought it off the internet, rather than letting the doc sabatoge that attempt. Of course I would need it long term if it worked, there could be supply issues. I'm just not sure if drugs like valproate or carbamazepine wouldn't make things worse.
So I've been thinking about phenazepam but I guess there are issues (including long term supply) and most of the literature is in Russian.
Well, the idea that you should be stable and healthy if at all possible is not something docs appreciate.
I don't have the genes for this kind of stuff (e.g. once I wake up I stay awake, preexisting tendency towards insomnia). Past 45 years old, age matters.
Anyway, not playing the pity card just providing a little background information.
Ideally, I'd get the best healthcare money could buy, but I don't have THAT much money ...
The worst drug in the world ... (I talked to an addiction doc but to them clonazepam is like methadone, and if there are problems with that they don't know what to do ..., and here 'detox' is diazepam for 6 weeks max).Last edited:Well it is known that some people have unusual difficulty switching from clonazepam to diazepam, clonazepam is not as inappropriate to taper as something like alprazolam but a problem is that small increments are not available in capsule form.
So when you tried tapering clonazepam before, I don't assume this problem with the increments was solved? If not, then you may have a better chance using a milligram scale to weigh parts of a capsule or tablet?
Yes phenazepam has longer halflife but can still cause cross-tolerance withdrawal from the part of the action that is different. Don't know why you would really need a lot of documentation on it, there are objections besides you personally have, like the high potential for amnesia or mental issues, although that does depend on your self-control with dialing in the dose and going higher or lower. If you transition it would be particularly dangerous, and if you don't transition I don't expect it to be that safe either compared to those CT concerns you have.
Have you tried contacting that detox center to ask what they do in certain situations like extreme insomnia and any other mental or physical health concern you might have, or about the inability of certain people to switch to diazepam (refer to the Ashton manual)?
Maybe the first part of the taper could be done at home and the very last difficult bit internal so that you have supervision to see it through. Just go very slow with the taper.
I doubt this will be of help to your situation, but my insomnia was nearly non-existent when I went to rehab but was very bad at home, made worse by what the stress in combination with being in that situation did to me, and my mental stability.
An advantage to first slowly switching to another benzo like phenazepam may be that you can first withdraw from the 'unique' effects clonazepam has on synaptic GABAergic firing patterns and then from the general benzo effect, allosteric enhancement of GABAaR. I guess indeed that maybe it would have to be another benzo than diazepam.'Have you tried contacting that detox center to ask what they do in certain situations like extreme insomnia and any other mental or physical health concern you might have' It's pretty much a matter of 'sign up first', go to the GP, or 'it's an addiction, right ? ' ...
As a 'side' note, someone pointed out to me that dopamine/achetylcholine imbalances are the endpoint of several diseases ...
I'm familiar with the effects of two antimuscarinic drugs (which helped with something, probably mostly by the action on acetylcholine, but also caused long lasting problems), bruxism, once when I tried diazepam: akathisia (which I may have so now and then on clonazepam), maybe some EPS-like symptoms, intestinal issues etc. once, when I had a combination of clonazepam and diazepam in my system I felt anticholinergic effects somewhat similar to promethazine, but weaker.
I 've though about taking something like levodopa ... alternatively, a dopamine agonist ... but I don't really know what I'm doing with that ... As far as underlying 'neurological diseases', it would be hard to distinguish them from the issues with clonazepam and I wouldn't really know what to look at. ? I don't have classical parkinson's.
TheTwighlight
Bluelighter
I have noticed, after 14 years on Klonopin & Xanax, that my dependence and tolerance to benzos has increased and seems permanent.
Back when I was younger I could take Klons for a month, then stop and be fine. Now, most recently, I took 4mg Klon/day for 2 weeks straight, then stopped and had 8 days of w/d. So, that's what I deal with these days. I also take Effexor XR, modafinil, gabapentin, and tramadol. I'm telling you, it's a badass combo but I don't sleep well at all anymore. I can stay awake for days with no obvious side effects, then I'll sleep a good night's sleep. I quit shooting heroin & meth about a month ago and my meds are now working very well.
I have no desire to be "sober" (look at my med list), but I do want to have a usable brain. Benzos help with this, very much so, but I have had just as much success with Effexor XR as an anti-anxiety drug as with benzos. I take Klonopin because to me it's the methadone of benzos, and I am a benzo addict to the nth degree. I quit Xanax in November '13, and have only taken it a handful of times since then, but I forever crave the "ahhhhhhhh......" relaxation euphoria of benzos. So I'm always on one now. I know the dangers & I know the benefits. But most people don't and they need to be educated. I take them for many reasons, primarily because I like the feeling & because I'm so psychologically hooked on the shit.
Like I said, dangers & benefits. Know them.
adder
Bluelighter
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It really depends on what you mean by a usable brain, but benzodiazepines generally give you the very opposite though after long-term use it may be extremely hard to notice how slowly your brain and memory function, I had no idea until I stopped, I'd never imagined I'd been so slowed down in everything. Long-term tolerance to benzodiazepines is also a thing, and at some point you may hit a dose from where there is no increase that could help you with decreasing effects due to tolerance, so you end up feeling worse and worse even though you're still on a high dose of a benzodiazepine, I'm sure a lot of people taking benzodiazepines at higher doses long-term get to that point but may not even realize, over the years for me benzodiazepines almost completely lost the ability to reduce anxiety, and the side effects kept increasing (take the lowest dose possible that helps you for as long as possible, losing efficacy happens much more quickly if benzos are abused rather than used). The benefits are none in my opinion, even if benzodiazepines are the only thing that can control your anxiety, they eventually lose efficacy which makes you end up in a situation when your anxiety becomes more unbearable than it was in the beginning and there is no medicine to put it under control. I've been there and trust me it's hell, even now 3 years from kicking clonazepam I often can't get my anxiety under control, I swore to myself I'd never take a benzo again, but on a few occasions in the recent months I did take a small dose of alprazolam (up to 1mg) which did virtually nothing for the anxiety but made me feel echoes of the withdrawal for a few days. Forget about any herbal medicines in such a situation, if they work in excessive doses, it's somehow through GABA as well and at times then they too seem to have side effects lingering for a couple of days. From this perspective it's pretty clear hanging on to benzodiazepines gives you no benefits long-term unless you consciously decide to stay on them forever, but then you do run a risk that at one point they stop working for you. I often do miss the anti-anxiety calm kick of benzos they gave me at the very beginning, but it's never coming back and either I break down completely or I learn to deal the anxiety myself and move on.
Anyway, good luck to you all.
